4 Physiology of Ventilation During Cardiac Arrest

Chapter 4 / Physiology of Ventilation 39 4 Physiology of Ventilation During Cardiac Arrest Andrea Gabrielli, MD, A. Joseph Layon, MD, FACP, and Ahamed H. Idris, MD CONTENTS INTRODUCTION HISTORY OF ARTIFICIAL VENTILATION AND CPR TECHNIQUES PULMONARY PHYSIOLOGY DURING LOW BLOOD FLOW CONDITIONS VENTILATION DURING LOW BLOOD FLOW CONDITIONS TECHNIQUES OF VENTILATION DURING CPR BASIC AIRWAY MANAGEMENT ADVANCED AIRWAY SUPPORT SPECIALIZED AIRWAY DEVICES IN CPR LARYNGEAL MASK AIRWAY COMBITUBE PHARYNGOTRACHEAL LUMEN AIRWAY TRACHEOSTOMY AND CRICOTHYROIDOTOMY ALTERNATIVE METHODS OF VENTILATION AFTER SUCCESSFUL ENDOTRACHEAL INTUBATION TRANSPORT VENTILATORS MONITORING VENTILATION DURING CPR CONCLUSION REFERENCES INTRODUCTION Ventilation—the movement of fresh air or other gas from the outside into the lungs and alveoli in close proximity to blood for the efficient exchange of gases—enriches blood with oxygen (O2) and rids the body of carbon dioxide (CO2)by movement of alveolar gas from the lungs to the outside (1). The importance of ventilation in resuscitation is reflected in the “ABCs” (Airway, Breathing, Circulation), which is the recommended sequence of resuscitation practiced in a broad spectrum of illnesses including traumatic injury, unconsciousness, and respiratory and cardiac arrest (CA). Since the modern era of cardiopulmonary resuscitation (CPR) began in the early 1960s, ventilation of the lungs of a victim of CA has been assumed important for successful resuscitation. From: Contemporary Cardiology: Cardiopulmonary Resuscitation Edited by: J. P. Ornato and M. A. Peberdy © Humana Press Inc., Totowa, NJ 39 40 Cardiopulmonary Resuscitation Recently, this assumption has been questioned and is currently being debated (2). Several laboratory studies of CPR have shown no clear benefit to ventilation during the early stages of CA (3–5). Furthermore, exhaled gas contains approx 4% CO2 and 17% O2, thus making mouth-to-mouth ventilation the only circumstance in which a hypoxic and hypercarbic gas mixture is given as recommended therapy (6). The introduction of the American Heart Association’s (AHA) Guidelines 2000 for Cardiopulmonary Resuscita- tion emphasizes a new, evidence-based approach to the science of ventilation during CPR. New evidence from laboratory and clinical science has led to less emphasis being placed on the role of ventilation following a dysrhythmic CA (arrest primarily resulting from a cardiovascular event, such as ventricular fibrillation [VF] or asystole). However, the classic airway patency, breathing, and circulation CPR sequence remains a fundamental factor for the immediate survival and neurological outcome of patients after asphyxial CA (CA primarily resulting from respiratory arrest). This chapter reviews pulmonary anatomy and physiology, early studies of ventilation in respiratory and CA, the effect of ventilation on acid–base conditions and oxygenation during low blood flow states, the effect of ventilation on resuscitation from CA, manual, mouth-to-mouth, and newer techniques of ventilation, and current recommendations for ventilation during CPR. HISTORY OF ARTIFICIAL VENTILATION AND CPR TECHNIQUES With the onset of CA, effective spontaneous respiration quickly ceases. Attempts to provide ventilation for victims of respiratory and CA have been described throughout history. Early descriptions are found in the Bible (7) and in anecdotal reports in the medical literature of resuscitation of victims of accidents and illness. Early examples of mouth-to-mouth ventilation are described in the resuscitation of a coal miner in 1744 (8), and in an experiment in 1796 demonstrating that expired air was safe for breathing (9). In 1954, Elam and colleagues described artificial respiration with the exhaled gas of a rescuer using a mouth-to-mask ventilation method (10,11). Descriptions of chest com- pression to provide circulation (12) can be found in the historical literature of more than 100 years ago. Electrical defibrillation has been applied in animal laboratory research since the early 1900s, and by Kouwenhoven in 1928 (11). The modern era of CPR began when artificial ventilation, closed-chest cardiac mas- sage, and electrical defibrillation were combined into a set of practical techniques to initiate the reversal of death from respiratory or CA. Resuscitation is associated with hypoperfusion and consequent ischemia. Recent studies suggest dual defects of hypoxia and hypercarbia during ischemia (13). Thus, the primary purpose of CPR is to bring oxygenated blood to the tissues and to remove CO2 from the tissues until spontaneous circulation is restored. In turn, the purpose of ventilation is to oxygenate and to remove CO2 from blood. The “gold standard” of providing ventilation during CPR is direct intubation of the trachea, which not only affords a means of getting gas to the lungs, but also protects the airway from aspiration of gastric contents and prevents insufflation of the stomach. Because this technique requires skill and can be difficult during CA, other airway adjuncts have been developed when intubation is contraindicated or impractical because of user skill. Before the arrival of an ambulance, ventilation given by bystanders must employ techniques that do not require special equipment. Manual methods of ventilation (i.e., the Sylvester method, the Shafer prone pressure method, and so on) consisting of the rhyth- Chapter 4 / Physiology of Ventilation 41 mic application and release of pressure to the chest or back and lifting of the arms had been in widespread use for 40 to 50 years prior to the rediscovery of mouth-to-mouth ventilation. These manual techniques were taught in Red Cross classes, to lifeguards, in the military, and in the Boy Scouts as recently as the 1960s, before being replaced by mouth- to-mouth ventilation as the standard for rescue breathing. Safar and Elam first showed that obstruction of the upper airway by the tongue and soft palate occurs commonly in victims who lose consciousness or muscle tone and that ventilation with manual techniques is markedly reduced or prevented altogether by such obstruction (14,15). Subse- quently, Safar and colleagues developed techniques that prevent obstruction by extending the neck and jaw and applying this in conjunction with mouth-to-mouth ventilation (16). Although mouth-to-mouth ventilation has been studied extensively in human respiratory arrest and has been shown to maintain acceptable oxygenation and CO2 levels, its evaluation in laboratory models of CA and in actual human CA has been limited. PULMONARY PHYSIOLOGY DURING LOW BLOOD FLOW CONDITIONS Effects of Hypoxemia and Hypercarbia on Pulmonary Airways During respiratory and CA, hypoxemia and hypercarbia gradually increase over time. The concentrations of both oxygen and CO2 affect ventilation and gas exchange. Hypox- emia has variable effects on airway resistance, which is the frictional resistance of the airway to gas flow and is expressed by: Airway resistance (cm H2O/L/s) = pressure difference (cm H2O)/flow rate (L/s) A number of studies in animals and humans, albeit with effective circulation, have shown that hypocapnia causes bronchoconstriction resulting in increased airway resistance, although the effect of hypercapnia on the airways is inconclusive (17–22). In one study, when end-tidal CO2 was increased from between 20 and 27 mmHg to between 44 and 51mmHg, airflow resistance decreased to 29% of the initial mean (17). However, other studies have shown that hypercapnia causes an increase in airflow resistance through a central nervous system (CNS) effect mediated by the vagus nerve (18–22). It appears that hypocapnia causes bronchoconstriction and increased resistance to flow through a direct local effect on airways, although hypercapnia causes increased airway resistance through action on the CNS (18–22). Hypoxic Pulmonary Vasoconstriction HPV is a physiologic mechanism that minimizes venous admixture by diverting blood from underventilated, hypoxic areas of the lung to areas that are better ventilated (23). Pulmonary vessels perfusing underventilated alveoli are normally vasoconstricted. This effect is opposed by increases in the partial pressure of O2. HPV matches local perfusion to ventilation, increasing with low airway PO2 and low mixed venous PO2. The greater the hypoxia, the greater the pulmonary vasoconstriction until a point is reached in which vasoconstriction becomes so intense and widespread that the response becomes patho- logic and pulmonary hypertension develops (24,25). HPV is inhibited by respiratory and metabolic alkalosis and potentiated by metabolic acidosis (26). Additionally, pulmonary vasoconstriction is more pronounced when pulmonary artery pressure is low and is attenuated by increased pulmonary vascular pressure 42 Cardiopulmonary Resuscitation (26). Hence, a consequence of low inspired O2 concentration, as occurs during mouth- to-mouth ventilation, could be decreased blood flow caused by increased pulmonary vascular resistance. Whether HPV occurs during CA and CPR is unknown, and warrants evaluation because hypoxemia occurs commonly. The Ventilation/Perfusion Ratio (V/Q Ratio): The Relationship of Blood Flow and Ventilation During Low-Flow Conditions During normal cardiac output, ventilation is closely matched with perfusion through a series of physiologic mechanisms exemplified by the maintenance of alveolar and arterial PCO2 within a range close to 40 mmHg at rest. However, during low blood flow states, the ventilation–perfusion relationship

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